Background and Objectives T cells require two distinct signals from antigen-presenting cells (APC) to become activated. The first signal, which confers specificity, is provided by the interaction of the MHC/antigen complex with the T-cell receptor (TCR). The second signal, which triggers clonal expansion, is provided by the binding of a co-stimulatory B7 molecule to its receptor on T cells. MHC/antigen-TCR binding in the absence of co-stimulation induces reversible, antigen-specific T cell anergy. We have previously reported that rhesus monkeys chronically infected with Brugia malayi displayed a polarized cellular response to B. malayi adult worm antigen (BmA). Cells from some infected animals responded in vitro to BmA (responder monkeys, RM) and cells from others did not (nonresponder monkeys, NRM). We showed that diminished production of Th1 cytokines (IL-2 and IFN- ) and lack of induction of IL-2R+ T cells may contribute to the unresponsiveness of PBMC from NRM to filarial antigen The objective of this research is to further our understanding of the mechanisms of T-cell unresponsiveness to filarial antigens in these animals, by assessing, by RT-PCR, the expression of the B 7.1 molecule in BmA induced PBMC. RNA from PBMC that had or had not been exposed to BmA or to Con A was assessed by reverse transcriptase polymerase chain reaction (RT-PCR) for the expression of the B 7.1 gene transcript. Results B7.1 mRNA expression was significantly induced in cells from three out of three of the RM (Mean of 36.00) and marginally in three out of six of the NRM (Mean of 2.56) Overall, B7.1 expression on cells from RM was 14-fold greater than those of NRM (P < 0.001). BmA did not induce B7.1 transcription in PBMC from the three control animals. Levels of mRNA for the B7.1 molecule in Con A-induced PBMC were not significantly different among the three groups of animals. These studies suggest that in addition to lack of induction of Th1 cytokines and underexpression of IL-2R, diminished expression of B7.1 could be an additional mechanism leading to antigen-specific unresponsiveness in rhesus monkeys with lymphatic filariasis. Future Directions To determine the roles that IL-10 and IL-12 may play in vitro in